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Effect of Black Tea Consumption on Intracellular Cytokines, Regulatory T Cells and Metabolic Biomarkers in Type 2 Diabetes Patients
Author(s) -
Mahmoud Fadia,
Haines David,
AlOzairi Ebaa,
Dashti Ali
Publication year - 2016
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5548
Subject(s) - foxp3 , glycated hemoglobin , medicine , il 2 receptor , endocrinology , type 2 diabetes , diabetes mellitus , immunology , regulatory t cell , peripheral blood mononuclear cell , glycemic , insulin , cytokine , t cell , immune system , biology , biochemistry , in vitro
The present study was undertaken to evaluate the effects of black tea intake on inflammatory cytokines and metabolic biomarkers in Type 2 diabetes mellitus (T2DM). Thirty patients with T2DM were randomly assigned either to a High Intake (HI) group, consuming three cups (600 mL) of black tea per day; and a Low Intake (LI) group, administered 1 cup (200 mL) per day, each during a 12‐week period. Intracellular cytokine expression, regulatory T cells (Treg), glycemic and lipid profiles were measured at baseline and following the tea intake period. Tea consumption correlated with major effects measured in peripheral blood of subjects that included significantly reduced glycated hemoglobin (HbA1c) levels, along with increased regulatory T cells CD3+ CD4+ CD25+ FOXP3, CD3+ CD4+ IL‐10+ cells (an immunosuppressive phenotype), reduced (pro‐inflammatory) CD3+ CD4+ IL‐17+ cells and reduced Th1‐associated CD3+ CD4+ IFN‐Υ+ cells. Tea consumption was also observed to abolish the significance of an inverse correlation between total serum cholesterol and representation of CD4+ IL‐4+ T cells, which may reflect protection against atopy‐related oxidative stress. Outcomes of this study describe both advantages and limitations to consumption of black tea as an aid to sustained health maintenance by persons at‐risk for TD2M and related obesity‐associated metabolic syndromes. Copyright © 2015 John Wiley & Sons, Ltd.

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